You can read the actual research as posted on the link below. But as a quick summary for non-technically minded people =>

Cleveland Clinic ran tests on various substances to determine their effect on the TMA lyase activity of common bacteria found in the human microbiome. Which is the medical jargon way of saying they looked at the bacteria that produces Trimethylamine (TMA) from different compounds like Choline and Carnitine, and introduced various chemicals to see how the process was affected.

Mice also produce TMA and oxidise this into Trimethylamine-N-Oxide (TMAO) like humans, so the tests were ran on them. They were divided into groups, some given high Choline diets, some not etc. They were then given a chemical called 3,3 DiMethyl-1-Butanol (DMB), which is actually a chemical analogue of Choline. The amount of TMA and TMAO was then measured in their urine. It was determined that the overall levels dropped, indicating that DMB inhibited the bacteria's ability to produce TMA from Choline and other substances.

To check their results, they took the bacteria from the microbiome and placed it in a dish. They measured the amount of TMA produced and the composition of the bacteria in the microbiome mix. They then reran the same experiment, adding DMB. On the second occasion, they noted that the bacteria species known to produce TMA had not been able to create TMA as before, had therefore died, and the composition of the bacteria had been altered from TMA producing bacteria, towards those that do not. This is a considerable step up from antibiotics, which essentially kills off all affected bacteria indiscriminately.

My understanding of the current state of this research is thus =>

DMB was objectively shown to prevent bacteria cleaving TMA from Choline and Carnitine. That's quite an achievement, because given to people who have issues with Trimethylamine, like us, it would prevent the bacteria producing smelly TMA and our problem would be virtually solved. As TMAO has been linked to atherosclerosis (a form of cardiovascular disease), given to those people DMB would help prevent heart disease.

Procter and Gamble were therefore interested in producing a pill form of DMB, which would help the aforementioned groups of people. HOWEVER, it was subsequently show that it would require a lot of DMB to induce these effects in humans, estimated at around 10-20 grams per day. Therefore P&G, although still interested in producing a pill, were looking for other chemicals with the same method of action but stronger in effect to make the pill more commercially viable.

Speaking as someone from an industry almost entirely based on intellectual property (semiconductor), the fact that a company has coughed up for the patent is very encouraging, as they are expensive at both the initial outlay and upkeep. If they are willing to invest money to protect this, it suggests they are actually taking this proposition quite seriously.